This article was originally published in a sponsored newsletter.
The role that eyelids play in the progression and treatment of dry eye disease is becoming more apparent with the shift from just aqueous deficient inflammatory-based dry eye to the mixed aqueous and evaporative components that cause increased osmolarity and inflammation, loss of homeostasis and surface damage.
In most cases, we treat inflammation reactively with steroids or immunosuppressives after dry eye has “grabbed hold” of our patients. This approach treats the inflammation that damages the cornea and inhibits the lacrimal functional unit (LFU) from providing good quality tears through an intricate neurofeedback loop that involves all of the tear-producing glands. We then see damage to the lid margins, especially to the meibomian glands and the meibum they produce. The compromised meibomian glands increase the evaporative aspect of tear depletion. This process explains how the mixed etiology of dry eye disease perpetuates the vicious cycle of inflammation. Even in Sjögren’s patients, who are the consummate aqueous deficient dry eye patients, we see the deterioration of the meibomian glands and the rise of the evaporative aspect of dry eye as the disease advances.
Regardless of whether the underlying cause is evaporative or aqueous deficient, anytime the loss of tears exceeds the supply, we have progressive mixed dry eye. We need to treat that inflammation as well as the damage to the cornea and tear-producing and tear-maintaining structures. We can decrease inflammation and increase tear production with immunosuppressives in a variety of molecules and unique delivery systems. Cyclosporine has been available for 21 years as an emulsion (Restasis) or for eight years as a lymphocyte functioning antigen antagonist that shows faster symptomatic relief (lifitegrast, Xiidra). More recently, the cyclosporine molecule has been wrapped with hydrophilic nanomicelle technology (Cequa) or perfluorobutylpentane (Vevye) to enhance penetration to the target tissue. These treatments fall under the “reactive” treatment modalities that clean up inflammation in the LFU.
We have several proactive treatments as well, when used earlier in the dry eye cascade. The first is a nasal neurostimulator (varenicline, Tyrvaya) that increases basal tear production within five minutes of the first application. We also have a tear preservation drug that instills a protective monolayer on top of the tear film, thereby reducing evaporative loss (perfluorohexyloctane, Miebo).
Dry eye disease is on a continuum as a combination of both evaporative and aqueous deficient components that perpetuate its progressive nature. Lid involvement is essential to the disease process, but our extensive armamentarium can help combat both inflammation in later stages and initial signs and symptoms.
